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Neuroradiology |
1 From the Departments of Radiology (H.P.M.v.H., J.A.V., T.T.C.O., J.C.v.d.B.), Clinical Neurophysiology (E.S.L., R.G.A.A.), Cardiology (S.M.P.G.E.), Neurology (H.W.M.), and Vascular Surgery (F.L.M.), St Antonius Hospital, Koekoekslaan 1, Postbus 2500, 3430 EM Nieuwegein (Utrecht), the Netherlands. Received July 31, 2001; revision requested September 24; revision received November 21; accepted January 8, 2002. Address correspondence to H.P.M.v.H. (e-mail: j.heesewijk@antonius.net).
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MATERIALS AND METHODS: Seventy-two consecutive CAS procedures were performed in 72 patients. Patients underwent neurologic examination before, during, immediately after, and 1 day, 3 months, and 1 year after CAS. MR imaging was used before and after CAS to assess the number of symptomatic and silent new infarctions. Two radiologists reviewed all pre- and postintervention MR images. The radiologists were blinded to the clinical data.
RESULTS: Postprocedural MR images showed new lesions on the side of stent placement in 11 patients. In six patients, the new lesions were clinically silent. Two patients had a major stroke, one had a minor stroke, and two had transient ischemic attack. In patients who had had transient ischemic attack or stroke before CAS, the frequency of new lesions at postprocedural MR imaging was higher (23%) than in asymptomatic patients (12%); this difference was not statistically significant (P = .29). There was no statistically significant correlation between embolic load as detected with transcranial Doppler US monitoring and the occurrence of either clinical symptoms or new lesions seen at MR imaging.
CONCLUSION: CAS is associated with embolic events. The majority of new lesions seen on postintervention MR images are not detected at neurologic examination.
© RSNA, 2002
Index terms: Carotid arteries, MR, 1722.121411, 178.121411 • Carotid arteries, stenosis or obstruction, 1722.721, 178.721 • Carotid arteries, transluminal angioplasty, 1722.1269, 178.1269 • Carotid arteries, US, 1722.12989, 178.12989
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Authors of some studies have documented the frequency of new lesions, presumably infarctions, at magnetic resonance (MR) imaging of patients after CEA (3,4). More recently, similar studies have been reported in the literature in which diffusion-weighted MR imaging was used (5–9). Enthusiasm for CAS has led to increasingly widespread clinical application of this endovascular technique (10). Although there are several studies in the literature of the incidence of cerebral lesions detected at MR imaging after manipulation of angiographic catheters in the carotid arteries (11,12), until now, to our knowledge, only one study of a small series of patients has been published that specifically assessed the safety of CAS by means of an evaluation of MR imaging findings after CAS (13). The purpose of our study was to assess, with MR imaging, the number and size of new brain lesions after CAS and to evaluate the association of these new lesions with neurologic deficits and transcranial Doppler (TCD) ultrasonographic (US) data.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Study Population
Fifty-six men (median age, 69 years) and 16 women (median age, 71.5 years) were included in the study. Fifty patients (69%) had experienced no symptoms. Twenty-two patients (31%) had experienced symptoms in the 12 months prior to CAS—eight patients had had a minor stroke, five patients had had transient ischemic attack (TIA), and nine patients had had ocular symptoms (eg, transient monocular blindness). The majority of patients had relatively high risk of complications if they were to undergo surgery due to cardiac and pulmonary comorbidity.
All patients had 90%–99% stenosis of the internal carotid artery. The degree of stenosis had been assessed with both intraarterial digital subtraction angiography and duplex US scanning before therapy. Furthermore, all patients had either documented progressive stenosis or severe four-vessel disease with insufficient collateral vasculature at color Doppler US and had to undergo major cardiac or vascular surgery. The majority of the asymptomatic patients had undergone placement of a carotid stent during the work-up for coronary artery bypass surgery.
The hospital human research committee approved this study, and informed consent was obtained from each patient.
Stent Placement
All patients were treated for stenosis of either the carotid bifurcation or the proximal internal carotid artery. In all patients, the stent in the internal carotid artery extended into the common carotid artery so that a portion of the stent rested in the external carotid artery (a technique we call "overstenting"). Endovascular treatment was performed by two experienced board-certified interventional radiologists (J.C.v.d.B. and T.T.C.O.) and one interventional cardiologist (S.M.P.G.E). The technique used is described amply in the literature (14,15). A femoral approach was used in all patients. In all cases predilation of the stenosis was performed with a balloon of 2.5–3.5 mm in diameter. After routine predilation, the stent was introduced, positioned, placed, and, finally, tailored. The postdilation diameter of the balloon was 5–9 mm, depending on the diameter of the artery as determined with duplex US prior to the procedure. In all cases a flexible, self-expandable stent (Easy Wall; Schneider, Minneapolis, Minn) was used. All 72 patients underwent angioplasty and stent placement without the use of cerebral protection devices.
Medication
All patients in our study received antiplatelet and antithrombotic drugs, including 250 mg/d of aspirin, 250 mg/d of ticlopidine (Ticlid; Sanofi-Winthrop, Maassluis, the Netherlands), or 75 mg/d of clopidogrel (Plavis; Sanofi-Winthrop), starting the day before the procedure. In addition, all patients received 6,000–8,000 IU of heparin (Heparine Leo; Leo Pharma, Breda, the Netherlands) intravenously during the intervention. Twenty-five patients also used anticoagulants. One milligram of atropine sulfate (Antonius Hospital, Nieuwegein, the Netherlands) was administered to reduce bradycardia and/or hypotension induced by compression of the carotid body before inflation of the angioplasty balloon.
Monitoring during Intervention
During the interventions, patients were continuously monitored by an independent neurologist and with TCD US of the ipsilateral middle cerebral artery so that any neurologic complications could be directly related to the phase of the intervention, brain perfusion, and embolic load. Systemic blood pressure, heart rate, and peripheral arterial oxygen saturation were routinely monitored as well.
MR Imaging
MR imaging examinations of the brain were performed 1 day before and 3 days after the intervention. MR imaging was performed with a 0.5-T system (T5 II; Philips Medical Systems, Best, the Netherlands) and a mirror head coil. The imaging protocol included a transverse T2-weighted spin-echo sequence (repetition time msec/echo times msec, 2,200/30, 90) and a fluid-attenuated inversion recovery (FLAIR) turbo spin-echo sequence (repetition time msec/echo time msec/inversion time msec, 6,500/120/2,000). The angulation of sections was bicommissural, with a section thickness of 6 mm, a gap of zero, a field of view of 230 mm, and a matrix size of 205 x 256 pixels. The sections used in the MR imaging sequences performed after the intervention were at the same levels as those used in the MR imaging sequences performed before the intervention.
Two neuroradiologists (H.P.M.v.H. and J.A.V.) simultaneously reviewed all MR images obtained before and after the interventions. Disagreement occurred in none of the cases. The radiologists were blinded to the clinical data, TCD US data, and examination date. The number, location, and size of the lesions were recorded. Lesions that had signal intensity characteristics equivalent to those of cerebrospinal fluid on T2-weighted images and were larger than 3 mm in diameter and lesions that were wedge shaped and cortico-subcortical were regarded as brain infarctions.
Evaluations before Intervention and during Follow-up
Patients were examined by an independent neurologist according to a standardized protocol that included neurologic examination, functional rating scales (Barthel Index, Rankin Scale), a memory test (the Mini–Mental State Examination), the National Institutes of Health Stroke Scale, and carotid duplex US scanning. These examinations were conducted before and directly after the intervention, during each of the first 3 days after the intervention, and 3 and 12 months thereafter. Signs and symptoms of any new neurologic deficit were recorded. Dependency in daily life was assessed with the Modified Rankin Scale. Stroke was defined as the occurrence of an acute focal neurologic deficit persisting for more than 24 hours. Strokes were considered major if patients had a Rankin score of 3 or higher at 3 months. A minor stroke resulted in a score of 0–2 on the Rankin scale.
Statistical Analysis
The Fisher exact test was used to analyze the clinical symptoms and the MR imaging findings. For data not normally distributed (eg, TCD US data) we used median and interquartile ranges for descriptive purposes and the Wilcoxon rank sum test for comparisons between groups. A value of P < .05 was considered to indicate a statistically significant difference.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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MR Imaging Findings
In 11 of 72 patients (15%; 95% CI: 7.9, 25.7) postprocedural MR imaging revealed a total of 19 new lesions. All new lesions were located on the side of the brain where a stent had been placed. In six patients these new lesions were clinically silent; the size of the lesions in this subgroup varied from 3 mm to 3 cm. Five patients who had new lesions on postprocedural MR images experienced adverse neurologic events during or immediately after the intervention; the size of the lesions in this subgroup varied from 3 mm to 7 cm. Two patients had a major stroke, one patient had a minor stroke (Figure), and two patients had TIA. In patients who had had TIA or stroke before undergoing CAS, the frequency of new lesions detected at MR imaging was higher (five patients [23%]; 95% CI: 7.8, 45.4) than in asymptomatic patients (six patients [12%]; 95% CI = 4.5, 24.3). This difference was statistically not significant (P = .29). Postprocedural clinical signs and MR imaging findings are summarized in the Table.
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Of the 11 patients with new lesions at postprocedural MR imaging, 10 had an acoustic window for TCD US monitoring. In these 10 patients, the median number of isolated emboli was 164.5 (interquartile range [IQR], 42–215), and the median number of embolic showers was 11 (IQR, 1–26). In the 54 patients without new lesions at MR imaging for whom TCD US data were available, the median number of isolated emboli was 103 (IQR, 69–155), and the median number of embolic showers was nine (IQR, 2–16). These differences were not statistically significant (P = .32 for isolated emboli and P = .90 for embolic showers).
In the group of patients that had new neurologic symptoms, 10 of 11 had an acoustic window. In this group, the median number of isolated emboli was 76.5 (IQR, 42–155), and the median number of embolic showers was 8.5 (IQR, 3–15). In the group of patients without new neurologic symptoms, 54 had an acoustic window for TCD US examination. The median number of isolated emboli in this group was 109 (IQR, 71–172), and the median number of embolic showers was 9.5 (IQR, 1–18). These differences were not statistically significant (P = .24 for isolated emboli and P = .88 for embolic showers).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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Noninvasive monitoring methods are desirable to establish the efficacy and safety of these endovascular procedures (13). During the interventional procedure, cerebral perfusion and embolism can be continuously monitored with TCD US of the ipsilateral middle cerebral artery. The embolic load during CAS, as documented with TCD US monitoring, is much higher in comparison with the embolic load during carotid endarterectomy (16). However, the neurologic complication rate is relatively low in view of this high embolic load. A possible cause of the relatively low number of neurologic deficits may be the extensive treatment of the patients with antiplatelet and antithrombotic drugs during stent placement.
On the basis of combined embolic and neurologic findings at TCD US, critical phases during the intervention have been identified. They include predilation of the carotid stenosis (especially after balloon deflation), stent placement, and tailoring of the stent.
In this study there was no statistically significant difference in the embolic load, as detected with TCD US monitoring, between the group with and the group without new lesions detected at MR imaging or between the group with and the group without new neurologic symptoms. Nevertheless, it seems reasonable to attribute these occurrences to embolic material.
It is difficult to compare the neurologic deficits in our group of patients treated with CAS with those occurring in patients treated with CEA. TIAs, which occurred in four patients in our group, and transient monocular blindness, which occurred in three patients in our group, are seldom diagnosed in patients treated with CEA because in most patients CEA is performed with general anesthesia.
Like the results of carotid surgery trials (17), the results of our study show that patients with symptomatic carotid artery stenosis seem to be at higher risk than asymptomatic patients of experiencing neurologic complications due to the intervention. In our group of 72 patients treated with CAS, 50 were asymptomatic. At our institution, asymptomatic patients are treated during the work-up for coronary artery bypass surgery. In patients with coexisting severe carotid and coronary disease, there is an increased rate of stroke during coronary artery bypass grafting (18,19).
In a large randomized trial (20), carotid endarterectomy was compared with medical therapy in patients with asymptomatic carotid stenosis. In patients with asymptomatic carotid stenosis of 60% or greater, this Asymptomatic Carotid Atherosclerosis Study reported an actuarially estimated 5-year risk of ipsilateral stroke or any perioperative stroke or death of 5.1% for patients who underwent surgery versus 11% (annual event rate of 2.2%) for patients who were treated medically. This results in an absolute risk reduction of 5.9% (1.2% per year) for patients who are treated with endarterectomy. In addition to the conclusions of the Asymptomatic Carotid Atherosclerosis Study, Norris et al (21) have reported that patients with asymptomatic carotid stenosis greater than 75% have a combined rate of TIA and stroke of 10.5% per year. These studies support the treatment of asymptomatic patients, although controversy on this subject certainly remains.
We used conventional MR imaging in the evaluation of our patients. The frequency and size of new lesions in our study may have been different if we had used diffusion-weighted MR imaging. As reported by Bendszus et al (11), findings from diffusion-weighted MR imaging show new brain lesions after angiography in 23% of patients with no apparent neurologic deficit. In their study, angiography was associated with a higher lesion rate in patients with a history of vasculopathy than in patients with no vascular risk factors. Our experience seems to support these findings.
The sensitivity of conventional MR imaging is relatively low in the early stages of cerebral ischemia. In the first 24 hours of the occurrence of cerebral ischemia, only 80% of conventional MR images show abnormalities (22). Because we were examining instances of both clinically apparent and clinically silent cerebral ischemia in which the time of occurrence was well defined, we decided to perform our postprocedural MR imaging examinations 3 days after CAS to ensure that the new lesions were as conspicuous as possible. Diffusion-weighted MR imaging, a more sensitive modality in early brain ischemia, was used by Lövblad et al (13) to evaluate 19 patients before and after CAS. They found new hyperintense lesions in five patients (26%).
Cantelmo et al (3) evaluated 76 patients who underwent CEA, performing an MR imaging examination before and after surgery. They found small areas of ipsilateral ischemic change on seven postoperative MR imaging studies (9%). Jansen et al (4) compared pre- and postoperative MR images obtained in 40 patients treated with CEA to detect intraoperative infarcts. Four patients (10%) developed new lesions that were seen at MR imaging; all of these lesions were clinically silent. Percutaneous angioplasty with stent placement is associated with a rate of microemboli that is more than eight times higher than that seen during carotid endarterectomy when percutaneous angiography with stent placement and carotid endarterectomy are evaluated with TCD US monitoring (16). In our study we saw new lesions at MR imaging in 11 (15%) of 72 patients; in six patients (8%)—the majority of those affected—these new lesions were clinically silent.
In comparing the neurologic complications seen in our study with those seen in a recent study conducted by Henry et al (23), some differences can be observed. Henry et al analyzed the results of 315 CAS procedures in 290 patients. Cerebral protection devices were used in 150 procedures. They observed the following periprocedural neurologic complications due to ischemia in 13 patients (4.2%): four TIAs (1.3%); four minor strokes (1.3%); and five major strokes (1.6%), including one death. In our study, four patients (5.6%) had TIA, two (2.8%) had minor strokes, and two (2.8%) had major strokes but no mortality. It should be noted that, unlike Henry et al, we did not use cerebral protection devices in any of our patients. In a group of 28 high-risk symptomatic patients with carotid artery stenosis evaluated by Malek et al (24), there were no minor strokes, one major stroke (3.6%), and three TIA (10.7%). The percentage of TIA and the percentage of stroke are both lower in our study.
It is difficult to make exact comparisons between the data of the current study and those of previously mentioned investigations. To our knowledge, few studies of the incidence of new lesions seen at MR imaging and neurologic deficits in patients after CEA and CAS have been published. Furthermore, the selection of patients (patients with serious cardiovascular comorbidity were substantially overrepresented) and the relatively small population in our study do not allow for a comprehensive comparison. More research into the safety and efficacy of CAS, as well as its long-term results, is certainly necessary before this procedure can be considered an alternative to CEA.
In conclusion, our data suggest that CAS is associated with a number of new hyperintense (ischemic) lesions at cerebral MR imaging, of which the majority are clinically silent; there does not appear to be a correlation between the occurrence of these lesions and the embolic load as evidenced with TCD US. In the future, the role of cerebral protection devices during CAS should be examined. These devices might lower the number of emboli.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Abbreviations: CAS = carotid angioplasty and stent placement, CEA = carotid endarterectomy, FLAIR = fluid-attenuated inversion recovery, IQR = interquartile range, TCD = transcranial Doppler, TIA = transient ischemic attack
Author contributions: Guarantors of integrity of entire study, H.P.M.v.H., J.A.V., R.G.A.A.; study concepts, H.P.M.v.H., J.A.V., E.S.L., J.C.v.d.B., T.T.C.O., R.G.A.A., H.W.M., F.L.M.; study design, H.P.M.v.H., J.A.V.; literature research, J.C.v.d.B., R.G.A.A., H.P.M.v.H.; clinical studies, S.M.P.G.E., J.C.v.d.B., T.T.C.O., H.W.M.; data acquisition, H.P.M.v.H., J.A.V., E.S.L.; data analysis/interpretation, H.P.M.v.H., J.A.V., E.S.L., R.G.A.A.; statistical analysis, H.P.M.v.H., J.A.V., R.G.A.A.; manuscript preparation, H.P.M.v.H., J.A.V.; manuscript definition of intellectual content, all authors; manuscript editing, H.P.M.v.H., J.A.V.; manuscript revision/review, H.P.M.v.H., J.A.V., R.G.A.A.; manuscript final version approval, H.P.M.v.H., J.A.V.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODS RESULTS DISCUSSIONREFERENCES |
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